Inhalation of asbestos and other mineral dusts leads to interstitial pulmonary fibrosis in animals and man. In previous work, we established the initial deposition sites and mechanisms of translocation of inhaled asbestos in rats. Now we demonstrate that a variety of dusts (i.e., chrysotile and crocidolite asbestos, fiberglass, silica, and Mt. St. Helen's Ash) exhibit a similar deposition pattern at the bifurcation of alveolar ducts. Only forty-eight hrs. after a one-hr. exposure to chrysotile asbestos, a significant lesion measurable by ultrastructural morphometry developed at alveolar duct bifurcations. The lesion is characterized by: 1) a thickened epithelium where numerous type I and type II cells contain abestos, 2) increased numbers of alveolar macrophages, and 3) an increased interstitial compartment consisting of fibroblasts, myofibroblasts and extracellular matrix. The lesion persists at bifurcations for at least one month and exhibits an increase in interstitial volume, comprised mainly of fibroblasts, macrophages and collagen. Interstitial intracellular microcalcifications containing asbestos have been identified at bifurcations as early as one month after a one hr. exposure, and these persist for at least five months post-exposure. The elemental content of asbestos is believed to play a significant role in its cytotoxic potential. Thus, we have carried out electron microscopic and X-ray analytical studies on chrysotile fibers which have resided in the lungs of rats through the five months period after a one-hr. exposure. We were surprised to learn that fibers in macrophages, epithelial cells, fibroblasts and interstitial connective tissue showed no significant changes in the ratio of magnesium to silicon when compared to fibers which had just been inhaled.